Demyelinating Syndromes in Systemic Lupus Erythematosus: Data From the "Attikon" Lupus Cohort.

central nervous system demyelination multiple sclerosis outcome demyelination in systemic lupus erythematosus systemic lupus erythematosus

Journal

Frontiers in neurology
ISSN: 1664-2295
Titre abrégé: Front Neurol
Pays: Switzerland
ID NLM: 101546899

Informations de publication

Date de publication:
2022
Historique:
received: 04 03 2022
accepted: 19 04 2022
entrez: 1 6 2022
pubmed: 2 6 2022
medline: 2 6 2022
Statut: epublish

Résumé

The demyelinating syndromes of the central nervous system (CNS) that occur in the context of systemic lupus erythematosus (SLE) may represent a manifestation of neuropsychiatric lupus (NPSLE) or an overlap of SLE and multiple sclerosis (MS). The differential diagnosis between the two entities has important clinical implications because the therapeutic management differs. To characterize CNS demyelinating syndromes in a large SLE cohort as neuropsychiatric SLE (NPSLE) or SLE-MS overlap using a multidisciplinary approach and existing diagnostic (for MS) and classification criteria (for SLE). Patients from the "Attikon" lupus cohort ( We identified 26 patients with demyelinating syndromes (3.7%). Of them, 12 were diagnosed as primary SLE-demyelination (46.2%) and 14 as overlap SLE-MS (53.8%). The two groups did not differ with respect to rheumatologic and neurologic manifestations or autoantibodies. SLE patients with demyelination manifested mild extra-CNS disease mainly involving joints and skin, while severe non-CNS manifestations were rare. However, these patients were less likely to have elevated IgG index (OR 0.055 95% CI: 0.008-0.40) and positive oligoclonal bands (OR 0.09 95% CI: 0.014-0.56), as well as brain lesions in the spinal cord, infratentorial, periventricular, and juxtacortical regions. A single brain region was affected in 9 patients with SLE-demyelination (75%), while all patients with MS-SLE had multiple affected brain regions. MS-SLE overlap was associated with an increased likelihood of neurologic relapses (OR 18.2, 95% CI: 1.76-188), while SLE-demyelination patients were less likely to exhibit neurological deficits (EDSS >0) at the last follow-up visit (50 vs. 78.6% in SLE-MS, respectively). Demyelination in the context of SLE follows a more benign course compared to a frank SLE-MS overlap. Extension of follow-up will ascertain whether patients with SLE-demyelination evolve to MS, or this is a

Sections du résumé

Background UNASSIGNED
The demyelinating syndromes of the central nervous system (CNS) that occur in the context of systemic lupus erythematosus (SLE) may represent a manifestation of neuropsychiatric lupus (NPSLE) or an overlap of SLE and multiple sclerosis (MS). The differential diagnosis between the two entities has important clinical implications because the therapeutic management differs.
Objectives UNASSIGNED
To characterize CNS demyelinating syndromes in a large SLE cohort as neuropsychiatric SLE (NPSLE) or SLE-MS overlap using a multidisciplinary approach and existing diagnostic (for MS) and classification criteria (for SLE).
Methods UNASSIGNED
Patients from the "Attikon" lupus cohort (
Results UNASSIGNED
We identified 26 patients with demyelinating syndromes (3.7%). Of them, 12 were diagnosed as primary SLE-demyelination (46.2%) and 14 as overlap SLE-MS (53.8%). The two groups did not differ with respect to rheumatologic and neurologic manifestations or autoantibodies. SLE patients with demyelination manifested mild extra-CNS disease mainly involving joints and skin, while severe non-CNS manifestations were rare. However, these patients were less likely to have elevated IgG index (OR 0.055 95% CI: 0.008-0.40) and positive oligoclonal bands (OR 0.09 95% CI: 0.014-0.56), as well as brain lesions in the spinal cord, infratentorial, periventricular, and juxtacortical regions. A single brain region was affected in 9 patients with SLE-demyelination (75%), while all patients with MS-SLE had multiple affected brain regions. MS-SLE overlap was associated with an increased likelihood of neurologic relapses (OR 18.2, 95% CI: 1.76-188), while SLE-demyelination patients were less likely to exhibit neurological deficits (EDSS >0) at the last follow-up visit (50 vs. 78.6% in SLE-MS, respectively).
Conclusions UNASSIGNED
Demyelination in the context of SLE follows a more benign course compared to a frank SLE-MS overlap. Extension of follow-up will ascertain whether patients with SLE-demyelination evolve to MS, or this is a

Identifiants

pubmed: 35645967
doi: 10.3389/fneur.2022.889613
pmc: PMC9131105
doi:

Types de publication

Journal Article

Langues

eng

Pagination

889613

Informations de copyright

Copyright © 2022 Nikolopoulos, Kitsos, Papathanasiou, Kapsala, Garantziotis, Pieta, Gioti, Grivas, Voumvourakis, Boumpas and Fanouriakis.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Dionysis Nikolopoulos (D)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Dimitrios Kitsos (D)

Department of Neurology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.

Matilda Papathanasiou (M)

Department of Radiology, Attikon University Hospital, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.

Noemin Kapsala (N)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Panagiotis Garantziotis (P)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Antigone Pieta (A)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Ourania Gioti (O)

Department of Rheumatology, "Asklepieion" General Hospital, Athens, Greece.

Alexandros Grivas (A)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Konstantinos Voumvourakis (K)

Department of Neurology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.

Dimitrios Boumpas (D)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Antonis Fanouriakis (A)

Rheumatology and Clinical Immunology Unit, 4th Department of Internal Medicine, Attikon University Hospital, Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Department of Propaedeutic Internal Medicine, Medical School National Kapodistrean University of Athens Medical School, Athens, Greece.

Classifications MeSH